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Open AccessJournal ArticleDOI

Anoikis molecular pathways and its role in cancer progression

Paolo De Paoli, +2 more
- 01 Dec 2013 - 
- Vol. 1833, Iss: 12, pp 3481-3498
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TLDR
Cancer cells develop anoikis resistance due to several mechanisms, including change in integrins' repertoire allowing them to grow in different niches, activation of a plethora of inside-out pro-survival signals as well as leading to metabolic deregulations of cancer cells.
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This article is published in Biochimica et Biophysica Acta.The article was published on 2013-12-01 and is currently open access. It has received 833 citations till now. The article focuses on the topics: Anoikis & Tumor microenvironment.

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Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Lorenzo Galluzzi, +186 more
TL;DR: The Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives.
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Oxidative Stress in Cancer.

TL;DR: During progression and metastasis, tumor cells adapt to oxidative stress by increasing NADPH in various ways, including activation of AMPK, the PPP, and reductive glutamine and folate metabolism.
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Matrix metalloproteinases (MMPs), the main extracellular matrix (ECM) enzymes in collagen degradation, as a target for anticancer drugs.

TL;DR: The main group of enzymes responsible for the collagen and other protein degradation in extracellular matrix (ECM) are matrix metalloproteinases (MMPs), and MMPs and their inhibitors have multiple biological functions in all stages of cancer development.
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Interplay between ROS and autophagy in cancer cells, from tumor initiation to cancer therapy

TL;DR: This review will focus on the regulatory role of reactive oxygen species (ROS) and autophagy levels during the course of cancer development, from cellular transformation to the formation of metastasis.
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Endoplasmic reticulum stress signals in the tumour and its microenvironment

TL;DR: How ER stress can influence not only the pro-tumoural features of cancer cells but also reprogramme the function of innate and adaptive immune cells, creating vulnerabilities that could be targeted by emerging therapeutic strategies is discussed.
References
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Journal ArticleDOI

Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery

TL;DR: It is shown that growth factor activation of the PI3'K/Akt signaling pathway culminates in the phosphorylation of the BCL-2 family member BAD, thereby suppressing apoptosis and promoting cell survival.
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AMPK and mTOR regulate autophagy through direct phosphorylation of Ulk1

TL;DR: A molecular mechanism for regulation of the mammalian autophagy-initiating kinase Ulk1, a homologue of yeast ATG1, is demonstrated and a signalling mechanism for UlK1 regulation and autophagic induction in response to nutrient signalling is revealed.
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Caspases: the executioners of apoptosis

TL;DR: The importance of caspase prodomains in the regulation of apoptosis is further highlighted by the recognition of adapter molecules, such as RAIDD [receptor-interacting protein (RIP)-associated ICH-1/CED-3-homologous protein with a death domain]/CRADD (caspase and RIP adapter with death domain), which binds to the prodomain of cspase-2 and recruits it to the signalling complex.
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Geometric control of cell life and death.

TL;DR: Human and bovine capillary endothelial cells were switched from growth to apoptosis by using micropatterned substrates that contained extracellular matrix-coated adhesive islands of decreasing size to progressively restrict cell extension.
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